Wednesday, December 25, 2013

A few days ago I tweeted a link to a blog post by the ASPCA’s Dr. Emily Weiss questioning the shelter dogma that animals should not be given as gifts. In this and an earlier post, Weiss describes her research which suggests that animals given as gifts are no more likely to be given up than animals not given as gifts. That article is open access, so you can read it and judge for yourself. It is a retrospective survey, so there is room for more rigorous science about this topic, but the paper definitely opens up interesting space for discussion and further investigation.

My bosom buddy Julie Hecht posted her thoughtful response on her Dog Spies blog and then ruminated more in a letter to her blogging pen pal Mia. Julie and I got into a conversation about it on Twitter, which unfortunately led to me ranting a bit (not in a hostile way, just in a “I thought about this all so much during my shelter medicine internship and I must let you all know everything I learned!” way). I’ve been thinking since then that 140 character spurts is not the best way to get across what I was trying to say.

Here is the story we tell ourselves about animal sheltering: there are irresponsible people out there. Lots of them. And they have animals, which they don’t value as animals deserve to be valued. They bring the animals to shelters, where people who care more and know more do their best to find the animals good homes. It is the job of the shelters to place these animals in the best homes possible, and to that end they should be very careful about every placement, because animals who have been abandoned once deserve never to be abandoned again.

There is a lot that is true in this story, mainly that animals do get the short end of the stick way too often and that, once abandoned, they absolutely deserve for the rest of their lives to be catnip and sunny couches or steaks and tennis balls. What I question is whether the shelter system that we are able to provide today is equipped to manage them well for long enough to find those homes, and whether shelter workers have the information necessary to predict what kind of home a particular adopter is actually able to provide.

Many, in fact most, shelters in this country are overwhelmed and are still euthanizing adoptable animals to provide space for more animals to come in. There are shelters for which this is not true, more and more of them every year. But they are the exception, and they tend to cluster in particular parts of the country. My friends in New England were shocked when I told them that during my internship I saw shelters where euthanizing healthy kittens for space was common. So given this situation, is it better to hold on to animals until you can find them the home that you think is perfect? Or is it better to take a chance and hope that you can get that animal out of a shelter which may have a 50% kill rate?

That leads us to the question of these lovely shelters which are able to place every medically and behaviorally healthy animal, and often even some not so healthy ones. These days there are plenty of those out there too. What should they think about animals as gifts?

I think that Dr. Weiss’s article makes the point that we aren’t really sure that we have all the information necessary to judge a particular adopter. I don’t think that this particular study makes an open and shut case. But I do think it provides evidence that this is a question worth asking. What do we really know about the home any adopter is going to provide? Is it worth denying an animal a potentially loving home because you don’t trust the word of the adopter?

In her post, Julie argued that there are some cases in which animals as gifts are particularly bad ideas, giving the example of bringing a puppy home to your grandmother who does not have the energy to deal with it. I agree. My suggestion is that shelters should consider moving to more case by case evaluations of particular adoptions, rather than operating on policies alone. If an adopter makes a good case, consider the adoption, even if they are planning to do something like give the animal as a gift. Keep an open mind about what constitutes a good home. But in the case where the adoption is patently a bad idea, then yes, talk the adopter through making a better decision, and refuse the adoption if need be.

In academic shelter medicine, where we like to think about changing everything about shelters because we don’t have to actually operate shelters, there has been a lot of discussion about this kind of change. Outdoor cats? No home visit prior to adoption? No adoption fee at all? Maybe those things are all good ideas. Maybe we really don’t know much about what makes a good adoption or a good home. We guessed, for years, and that was all we could do. But there is more and more research in the shelter community these days. We are starting to apply science (SCIENCE!) to these questions. I hope we can all both keep our minds open and evaluate the incoming research rigorously. It is a fascinating time for shelter medicine and shelter research; as one academic shelter veterinary specialist said to me, when I expressed shock at the overturning of some old principle or other, “Everything is on the table.”

Sunday, December 22, 2013

We’ve known for a while what kinds of dogs are at risk of biting humans: not any particular breed, but dogs who are not well socialized and not well cared for. Dogs living in houses with people are much less likely to bite than dogs living outside in yards or on chains.[1, 2] So why is this new paper about dog bite fatalities important?

Unlike previous researchers, who mostly approached the question of who gets bitten and what kinds of dogs bite by combing through old records, these authors monitored current events and followed up on every dog bite related fatality that was reported, for ten years (2000-2011). They interviewed law enforcement officers who were involved with these cases. They interviewed medical examiners and coroners. They followed current news articles about cases. This is all information that becomes very difficult to find when you’re trying to learn about a dog bite fatality years after the fact. As the authors write:

In our opinion, the present study represents the most comprehensive analysis of factors...associated with dog bites to date. Personal interviews with credible investigators were successfully conducted in 221 of 256 (86.3%) cases... Law enforcement personnel provide first-hand information not reported in the media and often identified errors of fact in the media reports.

Some information was still very difficult to obtain, and the most interesting part of the paper for me may have been the description of the lengths the investigators went to in their attempts to ascertain the reliability of reports of what breed some of these dogs were. They note that “the source of breed descriptors in media reports is usually unknown” and therefore not trustworthy. Interestingly, this paper never put that comment into context, but it is hard to read it without thinking about how challenging it can be to visually identify the heritage of a mixed-breed dogs, and all the implications that this has for news stories which seem to reflexively identify aggressive mixed-breed dogs as “pit bulls.”

In the context of the debate about whether pits get disproportionately named in media reports about dog aggression, this paper provides some interesting fodder. The authors calculated how often media reports contradicted each other: 21.6% of the time in reports about incidents involving single dogs, 36.4% in incidents involving multiple dogs. How often media reports differed from the animal control officer’s report: 34.9% in incidents involving single dogs, 43.3% in incidents involving multiple dogs. In the rare cases when a pedigree or DNA testing was available, that data disagreed with media reports in 7/19 cases for single dog incidents and 7/28 cases for multiple dog incidents.

What this paper found overall was mostly a vindication of what we already believed: there is no single factor that leads a dog to bite a human. But one very important factor is whether the dog is a “family” dog or a “resident” dog. The paper provides some lovely verbiage on the difference:

A resident dog was a dog, whether confined within the dwelling or otherwise, whose owners isolated them from regular, positive human interactions. A family dog was a dog whose owners kept them in or near the home and also integrated them into the family unit, so that the dogs learned appropriate behavior through interaction with humans on a regular basis in positive and humane ways.

Later in the paper, they add:

Dogs that are deprived of human interaction or direction are denied access to accurate information about appropriate behaviors with humans. Consequently, dogs in stressful, potentially dangerous situations or when maltreated may behave in ways primarily to protect themselves.

In other words, dogs who are not given a chance to learn how to interact appropriately with humans may not act appropriately with humans.

The rest of the paper is packed with nice statistics which I am not going to try to reproduce here. Suffice to say I expect to see excerpts from it on slides in presentations about canine aggression for years to come. I do want to explicitly point out that this paper only covered dog bite fatalities, not dog bites alone; fatalities due to dog bites are extremely rare (this paper found 256 in the United States over a 10 year period), whereas dog bites alone are quite common. I think it’s easy when reading this paper to want to extrapolate all this lovely data about the causes of fatal dog bites out to the causes of non-fatal dog bites. That’s understandable but a little dangerous: it usually requires repeated bites to kill a human, so I imagine such an attack to be different from the more common single bite. But I still believe all this data is very relevant to how we keep our dogs and how to prevent bites. The message the authors give is: be responsible with dogs and they will treat you well. Don’t, and you might be on dangerous ground.

Monday, December 2, 2013

I learned something new today about fearfulness, which it turns out has an even more complicated set of causes than I had previously known. And I had previously thought that fearfulness (made up of a whole lot of little genetic causes as well as almost impossible to fully comprehend environmental causes) was pretty damn complicated. The findings I’m going to describe are in mice, but this stuff is totally relevant to fearful dogs, at least in the opinion of this dog zombie.

My story begins earlier today when I received email from an ex asking if a recently published study is too crazy to be for real. (I do actually enjoy being the translator of Nature Neuroscience articles for the ex-boyfriends of the world.) My ex had encountered a National Geographic Phenomena article which covers the Nature Neuroscience article “Parental olfactory experience influences behavior and neural structure in subsequent generations." That is quite a title — let’s try it again. “When mice are trained to fear a particular smell, the brains and behavior of their offspring are affected.” (The Phenomena article, by the way, is detailed and provides some nice snippets of interviews with the researchers who did this study, but misses some of the nuances of the experimental setup. So while I do recommend you read it if you’re interested in this study, you should probably take it with a grain of salt.)

These researchers took a group of mice and fear conditioned them to the smell of a chemical called acetophenone. Then they bred them and tested their offspring. The offspring could detect acetophenone at lower concentrations than other mice; they had more receptors in their nose for detecting acetophenone than other mice did; and they were more reactive to loud noises after having been exposed to acetophenone. The smell was inherently scary to these offspring mice, even though they had not previously encountered it.

For the record, I am totally down with the first few changes. Offspring are adapted to the parent's environment by being better at smelling a relevant smell? Freaky as hell, but that is what epigenetics is and why we all find it so fascinating. But a change in behavior? That is beyond the usual freakiness of epigenetics. That's not just passing along more scent receptors for a particular smell. That's passing along the emotional content of the parent's experience with the smell. How is it possible!

Well, first, some details about the experiment:

How severe was the fear conditioning? Not all that severe, it turns out (which makes the results even more surprising to me). Mice were only trained over three days, with only five trials each day. A trial consisted of exposure to the odor, followed by a “mild” foot shock. I don't have a feel for how traumatic this experience was for the mice, and I'd be curious to know more. Was the shock really “mild”? You know, according to the mice, not according to the researchers, because we have all seen instances in which the animal's perception differs from the human's. Was being in the training chamber itself somewhat traumatic? Maybe the animals hadn’t been out of their home cages before. And so forth. But it was certainly a short period of training.

To test the startle response, the researchers put offspring mice into a startle chamber. The mice were habituated to the chamber for a few days before testing began. Then a few startle trials were run, in which the mice were exposed to sudden loud noises, and their responses were recorded. Next the mice were exposed to acetophenone, and then some more startling noises. The difference in their response was what was important: how much more did they startle after having been exposed to the smell, as compared to before exposure to it? Note that the mice were not actually startling just after exposure to the smell; there was a loud noise which triggered the startle. But they seem to have been primed by their reaction to acetophenone to startle more at subsequent noises.

Now, there are a zillion different possible explanations for why these mice could have appeared to be afraid of a smell that they had never encountered before. "Because my dad was afraid of it” is not the first thing that comes to mind, and the researchers tested a whole lot of other possibilities.

Were these mice particularly reactive to all smells? The researchers actually tested two groups of mice on two different smells. The group which was descended from mice trained on smell A reacted to smell A and not smell B. And vice versa for the other group. It really was just that particular smell.

Were these mice more anxious over all, possibly due to their father’s experience, having nothing to do with acetophenone? We might already have rejected this idea as the mice only reacted to the relevant smell, not the control smell. But the researchers also performed a test to see if the mice were particularly anxious over all, by examining the mice's fear of open spaces. The mice were no more afraid of open spaces than average, suggesting that they were not particularly anxious individuals in general.

Was there some social influence passed down from the fathers? The researchers had begun by fear conditioning male mice, who never had direct contact with their offspring, but did have direct contact with the mothers. It was possible that the fathers had somehow taught the mothers to fear the smell of acetophenone, and the mothers had passed this down to the offspring. To control for this, the researchers artificially inseminated some mice so that the females never interacted with the males, and had the offspring raised at an entirely different lab. They also fear conditioned mothers, and then fostered the offspring to mothers who had not been fear conditioned (and fostered offspring from normal mothers onto fear conditioned mothers). None of this changed the findings: the phenomenon appeared to be genetic, not social.

The researchers had chosen this particular smell because they knew what gene controlled the receptor for it. So they looked at the mice’s brains, and indeed the offspring of fear-conditioned mice did have more of the receptors for the relevant smell, which is why the mice were able to detect it at lower concentrations, even though they had never been exposed to the smell previously. Looking at the DNA for the gene controlling this receptor, they found epigenetic changes, specifically less methylation — basically, less stuff on the DNA, making it easier to express genes from. This is a plausible explanation for how the receptor changes happened.

Which means the story goes like this: mouse is trained to fear a smell; there are changes to the mouse’s DNA, marking a particular gene as one that should be expressed more often; these epigenetic changes are passed on to the mouse's offspring; that offspring generates more of a particular kind of smell receptor, because that gene is marked as “important, make lots!” And I am okay with that, as far as it goes. But how do we get from “make lots of receptors for this smell” to “when you smell this smell, be prepared for Bad Things to Happen”?

There is some precedent for this sort of thing, although it's limited. Primates are known to be primed to recognize snakes, although it's less clear if we are primed to fear them. Mice fed acetophenone while pregnant produced offspring who preferred the smell. Neither of these phenomena are epigenetic, which makes them inherently less freaky. It's particularly interesting to me that mice will “prefer” acetophenone if their mothers have eaten it: another case of inherited emotional content or salience, although in this case due to the in utero environement, not to epigenetics.

But in the end we don't really know how the salience of the smell was transmitted. More receptors for the smell don’t cause salience: just because you can smell it better doesn’t mean you’ll like or fear it. The researchers don't try to make a guess at how this happens, but they do comment on its importance for future research: “Such a phenomenon may contribute to the etiology and potential
intergenerational transmission of risk for neuropsychiatric disorders,
such as phobias, anxiety and post-traumatic stress disorder.” And dogs! Mice are actually probably a better model for dogs than for humans in this case, because dogs are so much more scent-oriented than we are.

So what does this mean for fearful dogs? We all want to know what makes a fearful dog fearful. How much of it is environment (poor socialization) versus genetics (starting life having been dealt a bad hand)? Well, first of all, remember that this was a very simple stimulus — a very specific smell and very straightforward classical conditioning. That’s why the researchers chose it. Could fear of the mailman be passed on as well? It would be harder, since there is not a single receptor to recognize the mailman, controlled by a single gene which can be expressed more frequently. (I love the idea of a mailman receptor, though.) So I wouldn't extrapolate these findings to non-scent stimuli quite yet. But that doesn't mean that this weird epigenetic force is not out there, interacting with the other poorly-understood forces of environment and genetics, in a crazy storm of things we can't separate out.

Sunday, November 10, 2013

So you have the full sequence of a couple few dog genomes, and a wolf genome to boot. (Yes, these days sequencing is cheap enough that genomics researchers can do this. There are more errors in these less expensive, “shallowly sequenced” genomes than the one that we use for the standard canine reference, but even with errors, you can still get the whole genome to play with.) So you have these genomes. And you are curious about domestication. What makes a dog different from a wolf? These genomes each are made up of millions of nucelotides, so when you do a straightforward comparison between dog and wolf, you get hundreds of thousands of differences in nucleotides, ranging from single nucleotides that are different to long stretches where chunks of the genome are repeated in one species but not the other. And what to make of the differences between pairs of dogs — are those important too? It can seem an overwhelming problem.

Luckily, in addition to having fast and cheap access to full genome sequences, we also have powerful computers for analyzing these sequences (and one of my favorite parts of my PhD program is that I get to use my programming skills in addition to my biomedical skills). What people do is think of patterns that suggest that certain areas are the interesting ones, and tell computers to look for those areas. It turns out that if you have a couple of genomes of animals of the same species, you can compare them to find regions where there is very little variation between animals. This suggests that this area is important — everyone has to have exactly the same sequence here, because anyone who has any differences is less fit and less likely to survive to pass on their genes. This is called a selective sweep, because at some point in the past, this change swept through the genome and everyone eventually got the identical copy of this region.

For an added bonus, if you have the ancestral species — in this case I am obviously talking about wolves, which are ancestral to dogs — you can compare this region in that species. If you find that this region is the same in all the dogs but different in the wolves, you have an area which is highly suspicious for being involved in domestication. So you can ask a computer to go find some of these low variation regions for you,

There are a lot of statistical tests that you can do to convince yourself that this area has sufficiently low variation to be interesting, but that area doesn’t, and it has been my pleasure this week to be reading about those in great detail. (Being a grad student rocks, but then sometimes there is statistics.) But the most recent papers I have been reading have pretty much done away with statistical tests to convince themselves that certain areas are involved in domestication. What they have done is to use stats to find areas that are just potentially interesting, and then they actually go look at the areas and see what they see. What known genes are in that area? Anything that could have to do with domestication? Yes? So let’s see how that gene differs in a whole bunch of dogs and wolves. The same in all the dogs, and different from that in all the wolves? Awesome. So what does this gene actually do? Can we understand how the genomic change between dogs and wolves — the mutation — changed the protein? Did it change the protein’s function? Or maybe dogs make more, or less, of that protein. Labs have just been selecting specific genes from these areas and investigating them intensely and seeing what they find out.

The best example of this approach (and the one I find the most interesting, because it was done in dogs, not pigs or chickens like the other papers I have been reading) was published early this year. You have probably heard it if you are interested in dog domestication, because it made a big stir by declaring that dogs had evolved to be better at digesting starch than wolves.

But when you read about this paper, did you know how they figured out that dogs are better at digesting starch? They did one of these low-variation genomic scans. They found some interesting regions. They looked at what genes were in these regions. They found a lot of genes involved in digestion, so they decided to chase that first. (They also found some interesting genes that work in the brain, and hopefully we will see a followup paper on that soon.) They focused on a few genes and tried to figure out what they did and how they had changed between dog and wolf. In at least one case they found that dogs just expressed a lot more of a particular protein than wolves do, and that protein is involved in digesting starch.

There are a lot more regions to look at in dogs, and there are some interesting things to hunt down in tame foxes, too, of course. We are in a fascinating time for genomics. The technology is becoming so inexpensive that we can actually look at the code of genomes belonging to individual animals more more readily than we could just a few years ago, and this is a game-changer. There should be many more discoveries to come soon about the mechanics of canid domestication!

Thursday, October 31, 2013

Despite my previous voracious reading about tame foxes, as I settle in to my new lab I’m realizing how much I don’t know about them. For example, one of the most interesting things about the tame foxes is that although they were selected just for behavior (not running away from a human approach), they have physical changes as well, and those changes mimic physical changes between wolves and dogs: the appearance of white patches of coat color, floppy ears, and curly tails. I have learned that this is not an example of white patches related to tameness:

Platinum fox

That is a platinum fox, a color morph unrelated to the white coat markings that seemed to appear with tameness. The white coat markings come from the star gene. So what do we know about the star gene? What do those markings look like?

I started my hunt for information about the star gene in my own reference manager, since I knew I had read about it before. The only paper I had saved about it was from 1981 (!) but it was written by the mastermind of the farm fox project, Dmitri Belyaev, so it seemed like a good enough place to start.

So back in 1981, when rock music was just starting to get really good, Belyaev was pondering the trickiness of the star gene. At that point, the tame fox project was only 20 years old. In 1969, the first white-spotted fox was born on the tame fox farm, with spots on his head and paws. Other foxes followed. The images from the paper show them looking like this (apologies for the poor image quality — it’s all I have to work with):

Fox kits heterozygous for star allele

This star pattern was not completely new. It had appeared on other fox farms, in foxes that were not selected for tameness. However, it was appearing much more often in foxes on this farm that were selected for tameness. In fact, the three families of foxes that were the most friendly to humans were showing this color pattern the most often. Unselected (not tame) foxes showed this star pattern 1.1% of the time, on multiple farms. (This includes foxes on the experimental farm which were from lines that were not selected for tameness.) Foxes in tame lines showed the pattern 3.7% of the time, or more than three times as often.

By the way, the fox kits shown above have only one copy of the star allele. Animals with both copies of this allele look much more like border collies:

But you can see how the non-white parts of their coats are a dark silver, unlike the platinum fox pictured at the top of this post.

Anyways, the question was: why were the tame foxes showing this pattern more often than conventional foxes? The pattern is particularly intriguing because it looks so much like the patterns we see in coats in domestic dogs, as well as in domestic horses and other domesticated animals. Was it possible that whatever mechanism was making these foxes more friendly to humans was also affecting their coat? The other explanation is just as likely but a lot less interesting: that when foxes were selected for tameness, the ones that were chosen just happened to have more copies of the star allele in their gene pool than average. Inbreeding would then cause this allele to show up more often.

Belyaev looked at family trees of foxes showing this pattern, trying to figure out if the gene for star pattern was recessive or dominant. The genealogy he found was somewhat perplexing. It didn’t follow the structure you'd expect for either a dominant or a recessive trait. The trait appeared to have variable penetrance, meaning that some animals with the star allele showed the star coat pattern, but some didn’t have star patterns, despite having the allele for it. This, of course, begs the question: if you have a group of animals, all of whom have the star allele, why do only some of them actually have the star coat pattern?

There are some possibilities:

There may be a hormonal difference in the tame foxes which changes the effect of the star allele. In other words, the hormonal soup of a tame fox (less cortisol, less adrenaline) may affect coat color during development, so that those foxes are more likely to express the star allele if they have it. Conversely, the hormonal soup of a conventional fox (more cortisol, more adrenaline) may somehow suppress expression of the white spotting.

The star allele has been around for a while, but perhaps it appeared in lower numbers in conventional foxes because it was somehow inactivated. Something about breeding for tameness may have activated the gene so that it was not “turned off” as often in tame foxes.

In 1981, no one knew which of these stories was more likely. This was before epigenetics was a hot topic, for one thing. But the nice part about reading historical papers like this one is that sometimes the answers to their questions exist in more recent literature. Which I am going to go hunt down now.

Monday, October 14, 2013

We often talk about the tame foxes as “silver foxes,” but in fact there are multiple color morphs in the tame population, not just silver. All of the foxes you’ll see here are the same species, Vulpes vulpes. The silver color morph was the color used for the first foxes which were selected for the creation of the tame population, but other morphs were brought in later.

Here is the silver morph, the color we are all most familiar with as being the color of a tame fox:

Tame silver foxes

My personal favorite fox color is Georgian white. The picture below is the one on my phone background.

Tame Georgian white fox

The ones that look so much like they have border collie markings, which are that lovely lighter silver color, are counterintuitively not called silver; they’re called platinum:

Tame platinum fox

And, of course, there’s the traditional red color, which somehow always surprises me the most to see on a tame animal:

Thursday, October 10, 2013

I finally got around to sharing the data from my study of dog salivary cortisol levels on figshare. I have meant to do this for months. Particularly, I wanted to do it so that I could wear the cool “I’m a figsharer!” t-shirt that Mark Hahnel gave me at scio13. How embarrassing would it be to wear that shirt and have someone ask what you shared and have to admit that you still haven't actually shared anything? But I am a figsharer now. So if you want numbers, go check it out.

Oh, and in case you’re interested in the associated paper, that’s here (but, sadly, not open access):

Friday, October 4, 2013

Having gotten somewhat settled in my new program, I asked my boss how she might feel about my blogging under my real name. She allowed as how that would be just fine. Hi, I'm Jessica. It's nice to meet you.

Which brings me to the really exciting part, which is that I also get to tell you guys that I am privileged to be training in a genetics lab which studies Belyaev's tame foxes! No, really. Where better to be for someone obsessed with the mechanisms behind domestication? We don't have a colony of the foxes here, sadly, but my boss goes to Siberia a few times a year and brings back genetic samples as well as astoundingly cute videos. The lab itself is plastered with photos of foxes playing with things. And the science, obviously, is extremely cool.

I am very lucky to get to work in a lab which works directly with canids. Until very recently, that was nearly impossible to do; in fact, one of the reasons I initially decided to get a DVM instead of a PhD was that I could not find a lab at the time (2007) that would let me work with canids. But dogs are finally getting to be a hot research topic, which has turned out very well for me.

Sunday, September 29, 2013

I was privileged to attend the 7th International Conference on Advances in Canine and Feline Genomics and Inherited Diseases this past week at the Broad Institute in Cambridge, Massachusetts. It wasn’t a large conference: about 150 dog and cat genetics researchers who get together every year and a half or so to catch each other up on what they’ve discovered recently, give each other suggestions about how to proceed or where to get good samples, and give their graduate students a chance to give some talks. I took notes on Twitter (#canfelgen) on my favorite talks (er, those of them that were not too technical; there were quite a few talks that I enjoyed hugely but that did not lend themselves to 140 character summaries). My apologies in advance if I got anything wrong; I was typing with my thumbs as fast as I could and may have made some mistakes.

Robert Wayne, Analysis of recent and ancient canine genomes suggest a new hypothesis for dog origins
Robert Wayne of UCLA talked about ancient canid genomes and “a new hypothesis for dog origins.” We are still not sure which gray wolf population was directly ancestral to modern dogs, and his work has shown that in fact no single population appears to fit the bill. Wayne believes that in addition to all the gene mixing between dog and wolves since domestication (which obviously muddies the picture), there was an ancient population of canids that gave rise to both dogs and wolves which we have not yet found samples from.

Wayne explained that ancient populations of wolves were much more diverse genetically than modern day populations, and we will really need to look to those ancient populations to solve the mystery of dog origins. About 10,000 years ago, populations of both wolves and dogs shrank dramatically in size, which explains why wolf populations are less diverse today than before that bottleneck. This was right around the time that domestication may have been happening, but we don’t know if the events are related.

So, based on this information, Wayne Lab embarked on a study of ancient canid DNA, comparing samples from dogs and wolves both from about 15,000-30,000 years ago. They found that the oldest dog populations were in Europe, not Asia. One interesting finding was in the black coat gene, which was relatively recently introduced from dogs into wolves and has swept through wolves. Apparently, being homozygous for black coat reduces fitness in wolves, but being heterozygous increases fitness. They don’t know why yet.

Wesley Warren, Genetic signatures of selection in the domestic cat lineage
Wesley Warren of the Washington University School of Medicine talked about using cats as models to study domestication. Comparing what we know about the behavior of cats to work in other species (dogs, horses, and chickens), he hypothesizes that cats aren’t actually undergoing significant domestication at all, because they are still very competent at living independently from humans and hunting their own prey. He talked about his work developing a SNP chip for cats, to aid in future genomic research in that species. A SNP chip is basically a library of known polymorphisms in the cat genome — single nucleotides that are known to differ between different individuals. Having all of these SNPs cataloged and available for use on a chip makes looking for correlations between these differences and things like behaviors or diseases much easier. At one point, his chip was used to discover the gene for curly coats in cats.

Warren talked about his recent work comparing the genomes of domesticated cats with their nearest wild relative. He found differences in RALY, a coat color gene. He found that cats have fewer receptors for smell than dogs do, but more for pheromones, and he wants to compare both olfactory and pheromone receptor genes in domesticated cats to big cats. He also talked about the 99Lives project, a project to get more cats sequenced (a theme which was returned to later in the conference).

Anna Kukekova, Simple behavioral pattern: is it simple?
Anna Kukekova of the University of Illinois talked about her work with tame foxes (if you don’t know about the Russian farm fox project, check out the excellent summary at the Thoughtful Animal). Kukekova opened by demonstrating the difference between the lines of foxes selected for tameness and the foxes selected for aggression with video in which a researcher performed a behavioral test on one fox from each line: first standing by a fox’s cage, then opening the door and reaching for the fox, then trying to pet the fox. The videos, shown side by side, were dramatically different: on the left, a clearly wild animal, both cowering from and menacing the human who stood near it. On the right, an animal reacting to human presence just as a dog in a shelter might, almost in a spasm of enthusiasm, wagging its tail, soliciting affection, rolling over to let the human pet its belly. Kukekova talked about analyzing the differences in behavior statistically, and how some of the most important behaviors they found for consistent differentiation between the populations were pricking ears forward, wagging tails, and approaching humans.

Kukekova investigated foxes which were second-generation crosses between tame and aggressive lines. The tame behavior was highly heritable, which was already known. Animals with heritage from both lines usually showed intermediate behavior, on the spectrum between tameness and aggression. What was interesting was that some of the crossed animals showed what she called “switching” behavior: the animals showed tame behavior at some points in the test, and aggressive behavior at others. For example, some of these animals were aggressive to humans who stood at their cage doors, but friendly when the door was opened. Others were friendly when the door was closed, but aggressive once it was opened.

Tara Baxter, Genomic approaches to identify putative canine behavior-associated genes
Tara Baxter of Cornell talked about her method of trying to track down some genes that are associated with different behaviors in dogs. This is a tough problem, as behaviors are usually influenced by multiple genes as well as by the environment, so tracking down a gene that influences aggression (for example) is a lot harder than tracking down a gene that is all by itself responsible for a disease. Baxter reviewed test results from owners who filled out a CBARQ (behavioral survey) about their dogs; she had access to a database of 19,000 surveys, so an impressive sample size. Using these tests, she averaged behaviors for each breed, getting a score of how likely animals of a particular breed were to display a particular behavior (for example, “begging”). Then she did an association study, using a canine SNP chip similar to the feline one discussed above. She used the chip to compare the SNPs found in individual dogs from various breeds, and looked for correlations between the average breed behaviors and the SNPs that she found in individuals of those breeds.

She had some interesting results which will benefit from more study. For example, for the behavior of urinating while left alone, she found an association in an area which is related to behavioral disorders in humans. Finding this association in an area which seems to affect behavior suggested to her that she might be on the right track, though of course a lot more work will need to be done. She mentioned some other interesting associations that she found as well. She also, of course, found associations that appear spurious, such as the association between a gene for long hair and chasing behavior. One amusing association she found was a relationship between the gene for short legs, such as you might see in a corgi, and a fear of stairs! She commented that sometimes physical traits explain behavior.

...And that is my smattering of summaries from the conference. Here’s hoping that I will manage to attend the next one, in eighteen months, in the other Cambridge — the one in the UK!

Monday, September 23, 2013

I've been thinking a lot lately about how dog aggression works, since the recent dog fighting bust (second largest in history). Fighting dogs are bred for willingness to attack other dogs, but for docility with humans. You don’t want your fighting dog to turn on you in the training yard or in the ring! Willingness to attack another dog, and to continue to attack when the other dog retaliates, is called “gameness.” Despite intense selection on the part of the dog fighters, the dogs show a lot of variation in levels of gameness: some dogs are very game and some are less so, even with training. But it does seem to be true that gameness is heritable, something you can breed for.

So how do you get aggression which is so specific? And what are the fighting dog breeders actually selecting for? What’s different in the DNA of a game dog and a not-game dog? We don’t have any real idea. Recently I came up with one possibility (too new even to be called a theory). It opens more questions than answers, but here’s the story.

There is a well-studied phenomenon in rats and mice related to the position of the fetuses in the uterus. (I know, uterine position is probably not related to genetics, but bear with me for a minute.) If a female fetus is surrounded by two males, one on each side, she gets more than her usual dose of testosterone in the uterus. Because testosterone helps the developing fetus know what sex to develop into, this extra testosterone makes her develop some masculine characteristics which will stay with her throughout life: she will be what is referred to as a masculinized female. Among other things, her behavior will be affected. Her play style will change to a more rough and tumble style. And she will be more aggressive towards others of her species.

This phenomenon has been demonstrated in multiple species, including guinea pigs, rabbits, and marmots. It is suspected to be in effect in dogs as well: although there are no published papers reporting on it in dogs (at least none that I could find — please let me know if I’m wrong!) I have heard it discussed at dog training seminars as a possibility. And given the range of species it affects and the similarity of effects of reproductive hormones on development across species, it seems really likely to affect dogs.

The big question is: how could this be a genetic phenomenon? The genders of your neighbors in the uterus are random, right? Well, not completely: one of the differences between masculinized and non-masculinized females is that masculinized females have more male offspring. Really. We don't know how that works, though there are some theories about why it may be a useful adaptation to some environments.

Moreover, testosterone doesn't just come from other fetuses. It comes from the mother as well. Some amount of testosterone is normal in development. What if what dog fighters are breeding for, without knowing it, is mothers who produce more testosterone when they are pregnant? Or maybe fetuses which are worse at transforming testosterone into estrogen (as fetuses like to do)? Or fetuses which are more sensitive to testosterone (maybe have more numerous or more sensitive testosterone receptors)?

These questions lead to even more questions, of course, which is why I haven’t even called these ideas a theory yet. Do the more aggressive masculinized female rodents show more aggression to their own species than to humans (which is my initial question about the fighting dogs)? Do male rodents with more males beside them in the uterus show increased levels of aggression? Do we know anything at all about different levels of testosterone released by the dam, not just by uterine neighbors?

There is a lot known about intrauterine position. It is really well studied, partly because it might help us understand the effects of reproductive hormones on fetuses in general, such as possible effects of artificial hormones which are unintentionally introduced into our diets, like BPA. So as I continue to read about it, I hope I’ll start to figure out if this is an idea with legs or just a passing fancy. In the interests of keeping this post readable, I haven’t written about all the interesting facets that I’ve encountered in this phenomenon, so feel free to ask questions. And there are certainly holes in the idea beyond the ones I mentioned, so feel free to point those out, too!

Edited to add: I messed up in suggesting that intra-uterine position might affect dogs the way it has been shown to affect rats, humans, and cattle. Dog placentas are fundamentally different from rat and human placentas, and also different from cow placentas (which form a third category). In short, it would be pretty unlikely for two fetuses to share hormones in-utero in a dog the way they can in rats, humans, and cows. So while I still think it's an interesting idea that a dog fetus could be exposed to different amounts of testosterone in-utero (probably due to processing of hormones by the placenta) and that this could affect its adult behavior, I want to emphasize that it is actually not likely that these hormones could be from other fetuses in a dog. The hormones would be from some difference in the mother, not from a chance alignment of the offspring. So in summary: if your bitch gives birth to one female and two males, that's not a reason to worry about masculinization and temperament in the female.

Monday, September 9, 2013

I finished my veterinary shelter medicine internship at the end of June. It was a crazy year. I learned so much, and I am so glad that I did it. I do feel that I did what I set out to do: learned a lot about the inner workings of animal shelters and made some very valuable contacts in the field.

I left the South and moved to the Midwest, where this fall I have started a PhD program. I'm working with a lab that focuses on the genetics of canid behavior and domestication (I know, right?). I'm so lucky that a place like this even exists. Sometimes I am frustrated that I found these interests in dog behavior and domestication so late in life, but then I remember that a few years ago, shelter medicine internships didn't exist, and there were no PhD programs studying canid behavior.

My life is very different right now compared to a few months ago. Instead of spending my days at chaotic shelters, I spend them alternating between lab work (so far, running PCRs) and lectures. Instead of having a highly organized schedule, everything is up to me: how many classes to take, how much to work in the lab, even what projects to work on in the lab.

So how will this blog's content change? I'm not sure yet. At a guess, I will write less about shelters, and more about the science behind behavior. I do hope to stay connected to the sheltering world in my Copious Free Time, though, so I may still write about that stuff. I'll see how my career here develops, and of course I am always open to requests from you guys!

Tuesday, August 27, 2013

On the face of it, the recent changes to Texas state law appear to be a good idea, aimed at preventing non-veterinarians from practicing veterinary medicine. But as is often the case with legislation, digging in to the situation a little deeper uncovers a load of unintended consequences, in this case in animal shelters. The whole story makes a great teaching case for how population medicine differs from individual medicine. There's a lot to cover, so let's get going.

The body of law in question is the Veterinary Practice Act. This Act
covers, you guessed it, the practice of veterinary medicine. Among the
basic rules that the Act lays out is the rule that in order for
veterinary medicine to be legally practiced on an animal, there must
exist a valid veterinary-client-patient relationship. That statement
takes quite a lot of unpacking, so here you go:

Veterinary medicine: in this case, giving a vaccination

Valid veterinary-client-patient relationship: the relationship
between the veterinarian, the client, and the patient. The veterinarian
must have actually met both the client and the patient. Usually this
must be renewed yearly -- so if you call your veterinarian and ask for a
refill on your pet's medication, but you haven't had your pet in to the
clinic for more than a year, the veterinarian must ask you to
bring your pet back in for a checkup, or the veterinarian is at risk of
losing their license. (Seriously. That's why they won't refill over the
phone after a particular period of time.)

But there is an exception made for herd health. If the veterinarian
is treating a herd of animals (commonly livestock such as cows) then the
relationship is with the herd, not the individual animal. So the vet
can prescribe treatments over the phone for a herd member that they
haven't ever seen, if they have recent experience with that herd as a
whole.

In the case of an animal shelter, some states treat animals in a
single shelter as a herd. This is entirely appropriate. In a shelter,
medicine should be practiced with the good of the population at heart,
not the individual animal. I promise that this is not as heartless as it
sounds, and ends up actually being better for the individual in the
end. If you let parvovirus get a hold in your shelter, it is the herd
that is sick, but it is individuals that die. It is best for individuals
to be in a healthy herd.

Until recently, the situation
in Texas was that it was legal for a non-veterinarian shelter employee
to give vaccines to animals in the shelter because they were members of a
herd, so the veterinarian could write general herd health protocols
("give the core vaccines to all animals at intake") without having to
see each individual animal. Now that's changed.

The
problem is with stray animals. Shelters don't own stray animals for the
first few days that they are in the shelter. This is called the animal's
"stray hold," and is intended to give the owner a chance to reclaim
their animal before it is put up for adoption. The number of reclaimed
stray animals is typically low, especially for cats; often only 2% of
stray cats are ever reclaimed. The majority of stray animals go on to be
owned by the shelter.

Texas has changed the wording of
their Animal Practice Act to specify that dogs and cats cannot be
considered herd animals. Yes, it has really taken me this much
explanation to get to the actual change in wording, but here it is: in
the middle of a definition of the veterinary-patient-client
relationship, the Act states (newly added text in italics):

A
veterinarian possesses sufficient knowledge of the animal for purposes
of Subsection (a)(2) [having a valid veterinary-patient-client
relationship] if the veterinarian has recently seen, or is personally
acquainted with, the keeping and care of the animal by:
(1) examining the animal; or
(2) making medically appropriate and timely visits to the premises on which the animal is kept. (NOTE: Per TAC 573.20(b) and 573.80(14), this section only applies to herd animals not including cats and dogs.)

On
the one hand, it does seem silly to think of a "herd" of dogs and cats.
But if you forget about the fact that the word "herd" has other
meanings in other contexts, the real question that this change in
wording is addressing is: Should shelters be allowed to practice
population medicine on their animals?

In this particular instance, the fallout goes like this:

By default, shelter animals in Texas cannot be treated as "herd" animals.

Animals which are owned by the shelter are exempt from the
Veterinary Practice Act, and therefore may still be treated as a herd.

Stray animals which are still in their stray holding period,
however, are not yet owned by the shelter and therefore are not part of
the shelter's herd.

Therefore, stray animals in their stray hold period must be examined
by a veterinarian before receiving any treatment, including initial
vaccines.

Not a big deal. Surely all shelter animals are examined by a veterinarian, right?

Actually, in quite a few shelters, veterinarians are only called in to treat sick animals, and the healthy animals are managed by technicians. Even in shelters which have a veterinarian, it is common for the veterinarian to only see sick animals. Of course, it is in the best interest of the animals for a veterinarian to see all of them as they come in the door, to establish a baseline of health status and to identify any problems that a technician might miss. But even in shelters with this policy, an animal may not be seen by a veterinarian for several days. Shelters are chronically understaffed and the vets are often behind on performing physical exams, as they have to prioritize treating sick animals more highly than checking on healthy ones.

Even in shelters which are fully staffed, it may be the next day before an animal is seen. If an animal comes in at the end of the day, the veterinarian may be in surgery the next morning and not get to physical exams until the following afternoon, so that the animal isn't seen for about 24 hours.

So the animal isn't seen by a vet for a day or three. If it's healthy, that shouldn't be a problem.

In the case of a shelter animal, one thing must happen the minute it comes in the door to the shelter: it must receive its vaccines.Prompt vaccination, right at the time of intake, is crucial in keeping animals healthy in shelters. Vaccination takes several weeks to bring the immune system up to its full efficiency in dealing with a pathogen, but there does seem to be an effect much earlier than that. Just a few hours one way or the other can actually make a difference, most critically in the very young and susceptible animals (did I mention in any previous posts how crazy kitten season can be in some areas?) and in the very dangerous diseases (such as parvovirus, which often simply manifests as dead animals with no warning). But don't take my word for it. The bible of shelter medicine, the Guidelines for Standards of Care in Animal Shelters, has this to say about prompt vaccination:

Because risk of disease exposure is often high in shelters, animals must be vaccinated at or prior to intake with core vaccines... Shelters that do not vaccinate with core vaccines immediately on entry, or do not vaccinate all animals, are much more likely to experience deadly outbreaks of vaccine preventable disease (Larson 2009).

This is how it works: the animal comes in to the shelter, either as a stray or surrendered by an owner. It gets processed, minimally receiving an identifying number, and is placed in a cage or run. Whoever performs this processing can either stick the animal with vaccines (and give it dewormers) at that time, or call a technician to do it. Giving vaccines isn't hard and you can train just about anyone to do it: it's technically easy (though it's nice to have someone else around to hold the animal still), and no decisions are really necessary. If the animal is too sick to receive its core vaccines against the most dangerous shelter diseases, it is too sick to be in the shelter and should get transferred to a hospital or other off-site care. Period. They all need their vaccines.

I'm saying this as someone who vaccinates her own animals much less often than conventional veterinary wisdom would have me do it. Shelters are full of disease and stress, and decisions about when and how to vaccinate there are going to be very different from decisions about animals in a home environment. I can't say it too often: without prompt vaccination, animals in shelters will die. The first question a shelter medicine specialist asks upon being confronted with an outbreak of parvovirus or distemper is "Are your animals vaccinated on intake?"

So, finally, on to this recent legal change in Texas. What shelter specialists see coming like an impending train wreck is lots of stray animals in Texas not getting seen by a veterinarian as soon as they are brought in to the shelter (it is not reasonable to expect that the vet could see them immediately); therefore, those animals not getting prompt vaccination; therefore, sick animals in shelters. Lots of them.

There is legal recourse at the city or county level: each city or county with a municipal shelter can change its ordinances to appoint the shelter the "designated caretaker" of stray animals during their hold periods. This allows the shelter to once again consider stray animals as part of the shelter herd, so that the veterinarian may ask someone else to give the vaccines before a physical exam has been performed. I have no real idea how likely it is that cities and counties will pass such ordinances, but I am guessing that the rate of adoption won't be anywhere near complete, and that the speed of adoption won't be blinding.

What's the moral of this story? I'm not really sure, but I think it has something to do with how complicated the consequences of legal wording can be, and how important it is to take the advice of specialists into account. I send my sympathies to Texas shelter veterinarians, who now will be faced with the scramble to still vaccinate stray animals on intake despite the change in laws.

Monday, July 15, 2013

Today I was privileged to visit Dr. Greg Berns' laboratory to see awake dogs in an fMRI. In vet school, of course I saw dogs getting MRIs of their brains as part of medical diagnostics, in hunts for cancer, stroke, inflammation, etc. But because an MRI requires that the subject hold perfectly still for several minutes at a time, these dogs were under general anesthesia, which is both expensive for the owner and physically difficult on the dog.

In humans, we can use the related technology, functional MRI (fMRI), to see changes in brain activity in response to different stimuli, such as music, smells, or looking at pictures. This is a useful tool in research, for example as we try to figure out which brain areas perform which tasks. In dogs, we haven't been able to do such studies, because the only way to keep dogs still enough for an fMRI has been to anesthetize them, and obviously a sleeping dog isn't going to have a meaningful reaction to external stimuli.

At Dr. Berns' lab, they have trained dogs to hold still in an fMRI machine while resting their chins on a chin rest. Can your dog hold its head perfectly still for minutes at a time? What about in a strange room, with loud machine noises all around, with ear muffs on to protect their hearing? It's an impressive feat, and done using entirely positive methods. (The training protocol was developed by Mark Spivak of Comprehensive Pet Therapy, Inc.)

I was most impressed by the dogs' relaxed body language. They entered the machine willingly, when their owners asked them to. They lay down with their chins on the rest and waited. As I watched from behind, I could see that many of the dogs were lying on one hip or even frog-legged, in very relaxed postures, suggesting that they were comfortable being in the machine. (Have you ever had an MRI? It is a claustrophobic experience. Humans getting MRIs would benefit from the extensive conditioning preparation that these dogs had, as well as having a loved one present to feed them treats periodically!) Some dogs would balk at some points and exit the machine, at which point their handler would ask them to return and they would. Dogs always had the opportunity to leave. At the end of the test, they came out happy and wriggly.

Highlights of the day for me:

The Boston terrier who hurled himself into the fMRI at full speed and then became rock-still for as long as his owner asked him to. That dog was committed to his fMRI experience! (Who would expect the Boston to be the calmest dog in the magnet?)

The dogs with their ear protectors wrapped onto their heads with an elastic material normally used to attach catheters and the like. They looked hilarious.

The treats fed to dogs on the end of long sticks so that they're easier to deliver inside the magnet. Ingenious.

Personally getting to participate in experiments by giving hand signals to dogs who were in the magnet, watching me intently as they waited for their treats.

The joke around the lab is that these tests will tell us why our dogs really love us: are we best friends or just food dispensers? It is a joke because of course fMRI is not a test for love; science has some trouble testing for squishy concepts like that. But fMRI does give us a new tool for guessing at what goes on in doggy heads, in addition to having to muck around with hormones like cortisol (as I have done) or strange little cognition tests like separation experiments or pointing experiments, as others have done. We have never been able to use this tool on awake animals before, so this is a huge step forward.

It was a fascinating day. I am deeply happy to see non-invasive research going on which takes the welfare of its canine participants into account, and waiting with bated breath to find out the results of the experiments I saw.

Thursday, July 11, 2013

I was just listening to a podcast about new health care technology using mobile phones. For example: someone wants to start eating healthier food. They install an agent on their mobile device which checks in with them every few days, asking things like How’s it going? Not so well? Why not? These agents are interactive, so if the user complains that things are not going well, it can understand the answer and reply: Here are some ideas to help you get past that particular hurdle. So I thought: why not for pets?
Imagine that when someone adopts a new dog (from a breeder or a shelter) they are asked if they’re willing to be signed up for a free preventive health care service. When they agree, they give their mobile phone number to the service. The shelter also provides some information about the animal: age, gender, if it is already spayed/neutered, and anything they think might need followup (such as if the animal is not housetrained, or if it is a jumpy-mouthy dog).

A week later, the new adopter gets a text message: How’s it going? Have you made your first vet appointment for Buster yet? No? Would you like some suggestions of veterinarians located near your home?

A few weeks later: How’s Buster? How is housetraining going? Not so well? Would you like some suggestions of dog trainers located in your area? The application might also alert the shelter that there is a training problem, so that the shelter can provide some followup if they have the resources.

And perhaps yearly: How’s Buster? Have you gotten his yearly checkup?

It would make an interesting study: are owners randomized into this service less likely to return their new pets than owners who are randomized out of it? How many owners continue to use the service (and how many request being removed from it)? Do owners find it helpful or annoying?
The first step, I imagine, is for me to do some reading on how these agents are implemented on the human side. I don’t know anything about this particular area, so anyone out there in internet land who has ideas for where to start (specifically, suggestions of peer-reviewed papers), they’d be welcome!

Sunday, June 9, 2013

I got a great question from Christopher of Border Wars on my last post. He wrote: “From the data I’ve seen, shelter intakes are dropping in real numbers and have been for decades despite constant growth in both population and animal ownership. So aren't the flood waters already going out?” I answered there, but have been feeling that there’s more to say on the topic.

As I wrote back to Christopher, the numbers of animals surrendered to shelters and the numbers of stray animals are definitely dropping in most (but not all) communities. Does this mean our work is done? Below you will find rampant over-generalization! Enjoy.

Location, location, location
Things are pretty good in the northeastern United States. When I started this blog, I lived in New England. Shelters there certainly had their problems, but they weren’t nearly as overwhelmed as the shelters that I have seen this year in the South. Northeastern shelters often import dogs (particularly puppies) from Southern shelters. So when you’re looking at intake numbers, think about what part of the country you’re in. The problems in the South are still intense, as I can attest from first-hand experience this year.

Dogs vs cats
When I was in New England, I observed that many shelters were managing their dog populations very well. Dogs in most shelters had a very high adoption rate there; healthy, behaviorally stable dogs in New England shelters had little to fear. Cats were an entirely different story. Plenty of shelters were euthanizing cats for space, and the others were stuck holding cats for months before finding homes for them.
Ironically, the tide is turning with the new programs in which cats who have been successfully following a healthy free-roaming lifestyle are simply sterilized, vaccinated, and returned to the neighborhood in which they were living. This has dropped cat euthanasia rates dramatically in participating communities. (See my previous post on leaving outdoor cats where they are.) You can’t really do this with dogs, so suddenly some shelters are finding themselves euthanizing more dogs than cats!

A dog problem or a pit bull problem?
I have been told that New England doesn’t have an unwanted dog problem, but it does have an unwanted pit bull problem. By that, of course, I mean pit bull type dogs, as the “pit bull” designation does not refer to a specific breed and is often used loosely to describe mixed-breed dogs who have a certain look.

For sure, in almost any shelter you go to, you’ll see many more pit bull types than dogs of any other breed. (The exception is shelters in communities with breed specific bans, in which those types of dogs may not be allowed in the shelters, or are immediately shipped out or euthanized.) This type of dog is harder to adopt out of shelters, as many adopters are looking for a different type of pet. They also do poorly in shelters, because they are highly social, smart, and energetic. Many shelters are specifically struggling with how to stem the flood of pit bull type dogs; the various programs that have been tried are a topic for a different post.

Some improvement is not enough

And finally, as I said to Christopher in my answer to his comment, we may have seen some improvement, but it is nowhere near enough. Appalling numbers of animals were euthanized in shelters in the past. Somewhat less appalling animals are euthanized now. The Humane Society of the United States estimates that the numbers have dropped from 12-20 million shelter euthanasias per year in the 1970s to 2.7 million shelter euthanasias today. It’s all guesswork, because there is no centralized reporting for animal shelters; we don’t even know how many shelters are in the U.S., let alone how many animals they process and how many animals survive. Remember, though, that those numbers don’t include animals trapped in inhumane conditions in long-term facilities, sometimes for years (again, this is from personal experience). It does not account for overcrowding at shelters causing welfare problems, even short-term, for the animals who stay there. Nor does it account for animals dying of disease in shelters which do not have the resources to manage their populations. And it probably accounts for spectacular changes in some shelters, but much less change in others.

The trend is in a good direction, but we’re not done, and the trend won’t continue in this direction without more work. So get your animals spayed or neutered, don’t buy animals from pet stores or flea markets or online, take your dog to a training class to prevent behavior problems, exercise your dog for the same reason, and volunteer at your local shelter.

Saturday, June 8, 2013

This past week I was at one of the largest shelters in the United States. At one point, I was standing by a door chatting with some of my co-workers for ten minutes, and during those ten minutes we saw three sets of people coming in to surrender their dogs. This shelter takes in about 100 animals a day, 30,000 animals a year.

My co-workers and I realized that the biggest problem this shelter faced was its massive intake. Nothing else they could do to solve their problems would be more effective than reducing that. In fact, it has been shown again and again that euthanasia in shelters mirrors intake: more intake means more euthanasia, and less intake means less euthanasia. But how do you reduce intake?

When I was catching up on my life this morning with my husband, I told him about managed intake: the shelter only accepts owner-surrendered animals that they have room for. If they don’t have space, they don’t accept the animal. The animal may be put on a waiting list, and ideally the shelter offers support during the wait (food if the owner can’t afford to feed the animal, behavioral advice, help finding animal-friendly housing).

In the case of animals that the shelter knows that they will have great difficulty placing (old, sick, etc.), they will let the owner know that they will immediately euthanize the animal. This sounds cold, but the alternative that many shelters practice is to take the animal in and euthanize it without warning the owner that this is inevitable. (No one likes conflict, least of all institutions run by local government.) This approach shifts the responsibility onto the owner. Although many people who surrender animals to shelters know that the animal may be killed, it is much easier to convince yourself that that could never happen to your animal (which you know is so wonderful) if there is some chance that the animal will survive. This puts the choice of euthanasia onto the shelter, and the blame onto the shelter. But moving the decision back to the owner means that the owner has to deal with the decision, and hopefully find another solution, or at least take the experience into account the next time they acquire an animal or have difficulties with a pet. (Is the experience of surrendering a pet to an unknown fate more difficult than the experience of having a healthy pet euthanized? I have my own guess, and you can make yours.)

My husband (kindly playing the foil in the Socratic dialogues of this blog) asked me about the unintended consequences of such a policy. The shelter is mandated by the county to accept stray dogs. Will the policy result in more people untruthfully representing their surrendered pets as strays? Will it even result in more animals being abandoned on the street?

We don’t know; the research hasn’t been done. Some shelters have experimented with managed intake, and their experience has been that this policy does not actually cause very many people to do reprehensible things. Mostly, people will put their animals on the waiting list (perhaps with some yelling at the shelter employees first), and then some of them will surrender the animal when room is available, and some will find other options (like a friend who wants a dog), and some will decide to keep the animal after all. And some will be lost to follow up, so perhaps those people do put the animal on the street.

But here is what I think about it: abandoning an animal on the street is illegal. So if a shelter institutes managed intake, and as a result some people break the law, whose fault is that? Is it the shelter’s fault? In my book, the shelter is behaving very responsibly by refusing to accept animals that they cannot care for, and by being honest that a new animal which is accepted must be euthanized. Some support for owners who need it is essential, and should be considered a part of managed intake. If an owner responds to this policy by breaking the law, I feel that the blame is with them. Perhaps increased enforcement of animal cruelty laws (which include neglect) is the proper answer to this problem.

More and more shelters are considering managed intake. I think there will be anger in some communities at first, but I am very hopeful that if enough shelters institute this policy, there will eventually be a sea change in our culture’s approach to unwanted animals. Whose problem is an unwanted animal? The owner's.

Tuesday, June 4, 2013

I am totally digging the first week of Social Epidemiology, a course on Coursera. (Quick summary of Coursera: free classes; you don’t have to commit, can just watch the lectures if that’s all you want; entirely online and open.) Epidemiology is of course the study of disease at a population level, and most people think of classic epidemiology cases like Ebola virus (who got it first? how is it transmitted in the population? who’s most at risk? how do we stop its spread?). But social epidemiology is about the social factors in disease — most commonly chronic diseases like diabetes and heart disease. What social factors cause people to live unhealthy lives?

This is obviously applicable to veterinary preventive medicine (though not directly addressed in the class; it takes some extrapolation). Why don’t people vaccinate their animals? Why don’t they exercise their animals? My personal interest is in how to prevent these sorts of problems, so I’m very much hoping that later in the class it will address preventive medicine and policy (how do we help people live healthier lives?). But if I wait until that happens to recommend it, it will be too late! Take it now! No committment! You can just listen to the lectures (or just do the readings). Only take the quizzes if you want to (though the first one wasn’t difficult). Just learn!

Hopefully a few years from now I will be offering the world’s first Social Veterinary Epidemiology class online. A girl can hope.

Sunday, May 26, 2013

I was on the phone with my mom yesterday, and she asked what I was doing next week. “Going to a large shelter in [big Southern city,]” I say.

“I’m not sure what the point of all this is,” says my mom with her PhD, who had been so enthusiastic when I told her that I was planning to do a PhD in the genetics of dog behavior after I finished my internship. “But you have known what you’re doing before, so I guess you do this time too.”

“Do you want me to try to explain it?” I ask, and she allows that this would be acceptable.

So I try to explain why I’m doing a year of clinical work in shelters if I am so interested in dog brains. The thing is that I have always been interested in both research (and teaching and writing peer-reviewed papers and being hidden in the ivory tower) and in being in a shelter or in the field and getting my hands dirty and making a tangible difference. I do want to figure out the mechanisms behind pathological fearfulness in dogs, and what makes domesticated animals like dogs different from wild animals like wolves. But I also want to keep connected to the world of the animals who are actually suffering from shyness, both so I can get new ideas about what needs studied, and so that I can try to apply some of what I learn.

I have always felt that my two interests, in fearfulness in dogs and in clinical shelter behavior, are closely intertwined. But the institutions I’ve learned from don’t seem to see it that way. Four years of clinical work for a DVM degree (in which we were told again and again that more veterinarians are needed in research, but in which we had no classes about research topics). One year of a research Masters. One year of a clinical internship. Next, several more years of research. My internship mentors worry that I am too interested in research and not enough in clinical work. My PhD mentor worries that I am too interested in clinical work and not enough in research. When do I get to do both at once?

After I’m done with schooling, maybe. I’ve learned a lot about how shelters work in my internship, and maybe even more importantly, I’ve seen some possible career paths in consulting for me. Part time work, called in on a temporary basis to work for large animal welfare groups dealing with issues such as enrichment in temporary shelters after large seizures of hundreds of animals, or behavioral evaluations of large numbers of seized fighting dogs. The other parts of my time spent teaching? Doing some research? It’s way too soon to try to figure out the details, but at least I have ideas of where to look to put together my perfect patchwork of jobs. And hopefully with my internship under my belt I will have the street cred to say that I know how shelters work and what their common problems are.

Maybe I should have just said that there are lots of broken dog brains in shelters, and left it at that!

About the Dog Zombie

Jessica Perry Hekman, DVM, PhD is fascinated by dog brains. She is a postdoctoral associate at the Broad Institute of MIT and Harvard, where she studies the genetics of dog behavior. Her interests include the stress response in mammals, canine behavior, canine domestication, shelter medicine, animal welfare, and open access publishing. You may learn more about Jessica at www.dogzombie.com, or email her at jph at dogzombie dot com. All opinions expressed here are her own.

For the animal shall not be measured by man… They are not brethren, they are not underlings: they are other nations, caught with ourselves in the net of life and time, fellow prisoners of the splendor and travail of the earth. (Henry Beston)